Our laboratory has continued to study the central nervous system effects of endogenous peptides, most notably neurotensin and thyrotropin-releasing hormone. In the past year we have made several potentially important findings. First, neurotensin injected into the cerebroventricular system of rodents produces a potent hypothermia; this effect is not due to the peptide producing a poikilothermic state and therefore differs from the effects of other peptides such as bombesin and beta-endorphin. We have continued to obtain data consistent with the view that neurotensin interacts with brain dopamine systems, in particular the mesolimbic dopamine system. When neurotensin is injected directly into the nucleus accumbens, a major termination site of this mesolimbic dopamine system, it produces: (1) blockade of amphetamine-induced locomotor hyperactivity and rearing and (2) diminution in the rate of rewarding brain stimulation from the A-10 dopamine cell bodies in the ventral tegmental area, the origin of the mesolimbic dopamine system. Furthermore, neurotensin also inhibits avoidance responding but not escape responding in a discrete trial active avoidance paradigm. These three effects of neurotensin, along with others previously elucidated, are also characteristics of neuroleptic (antipsychotic) drugs. Since the mesolimbic dopamine system has been postulated to play a role in the etiology of schizophrenia, it is possible that neurotensin, which is present in neuroanatomical proximity to this dopamine system and, as noted, possesses several properties in common with antischizophrenic agents, may play a role in the etiology of certain mental disorders.